Metabolic bases of excess post-exercise oxygen consumption: A review

Abstract

The classical “oxygen debt” hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2consumption in excess of resting that occurs after exercise. The O2debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between intial, fast (“alactacid“), and second, slow (“lactacid”), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a “reservoir of carbon,” which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2may be understood in terms of those factors which directly or indirectly influence mitochondrial O2consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term “O2debt” be used to describe a set of phenomena during recovery from exercise. The terms “alactacid debt” and “lactacid debt,” which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., “excess post-exercise oxygen” consumption“ (EPOC) and ”recovery O2“ will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

abstract = "The classical “oxygen debt” hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2consumption in excess of resting that occurs after exercise. The O2debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between intial, fast (“alactacid“), and second, slow (“lactacid”), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a “reservoir of carbon,” which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2may be understood in terms of those factors which directly or indirectly influence mitochondrial O2consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term “O2debt” be used to describe a set of phenomena during recovery from exercise. The terms “alactacid debt” and “lactacid debt,” which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., “excess post-exercise oxygen” consumption“ (EPOC) and ”recovery O2“ will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.",

N2 - The classical “oxygen debt” hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2consumption in excess of resting that occurs after exercise. The O2debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between intial, fast (“alactacid“), and second, slow (“lactacid”), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a “reservoir of carbon,” which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2may be understood in terms of those factors which directly or indirectly influence mitochondrial O2consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term “O2debt” be used to describe a set of phenomena during recovery from exercise. The terms “alactacid debt” and “lactacid debt,” which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., “excess post-exercise oxygen” consumption“ (EPOC) and ”recovery O2“ will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

AB - The classical “oxygen debt” hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2consumption in excess of resting that occurs after exercise. The O2debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between intial, fast (“alactacid“), and second, slow (“lactacid”), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a “reservoir of carbon,” which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2may be understood in terms of those factors which directly or indirectly influence mitochondrial O2consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term “O2debt” be used to describe a set of phenomena during recovery from exercise. The terms “alactacid debt” and “lactacid debt,” which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., “excess post-exercise oxygen” consumption“ (EPOC) and ”recovery O2“ will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.